Ccrl2 deficiency deteriorates obesity and insulin resistance through increasing adipose tissue macrophages infiltration.
Ccrl2 deficiency deteriorates obesity and insulin resistance through increasing adipose tissue macrophages infiltration.
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Ccrl2 缺陷通过增加脂肪组织巨噬细胞浸润而恶化肥胖和胰岛素抵抗
DOI：
10.1016/j.gendis.2020.08.009
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发表时间：
2022-03
期刊：
影响因子：
6.8
通讯作者：
Li X
中科院分区：
文献类型：
--
作者：
Xu M;Wang YM;Li WQ;Huang CL;Li J;Xie WH;Zeng HX;Tao LF;Li X
Obesity-induced inflammation, characterized by augmented infiltration and altered balance of macrophages, is a critical component of systemic insulin resistance. Chemokine-chemokine receptor system plays a vital role in the macrophages accumulation. CC-Chemokine Receptor-like 2 (Ccrl2) is one of the receptors of Chemerin, which is a member of atypical chemokine receptors (ACKR) family, reported taking part in host immune responses and inflammation-related conditions. In our study, we found ccrl2 expression significantly elevated in visceral adipose tissue (VAT) of high fat diet (HFD) induced obese mice and ob/ob mice. Systemic deletion of Ccrl2 gene aggravated HFD induced obesity and insulin resistance and ccrl2−/− mice showed aggravated VAT inflammation and increased M1/M2 macrophages ratio, which is due to the increase of macrophages chemotaxis in Ccrl2 deficiency mice. Cumulatively, these results indicate that Ccrl2 has a critical function in obesity and obesity-induced insulin resistance via mediating macrophages chemotaxis.
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